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Okamoto Mariko

Affiliate Master Yamaguchi University

Antioxidant, N-acetyl-L-cysteine inhibits the expression of the collagen α2 (I) promoter in the activated human hepatic stellate cell line in the absence as well as the presence of transforming growth factor-β

Hepatology research : the official journal of the Japan Society of Hepatology Volume 24 Issue 3 Page 305-315
published_at 2002
Title
Antioxidant, N-acetyl-L-cysteine inhibits the expression of the collagen α2 (I) promoter in the activated human hepatic stellate cell line in the absence as well as the presence of transforming growth factor-β
Creators Segawa Makoto
Creators Kayano Kozo
Creators Sakaguchi Eiki
Creators Okamoto Mariko
Creators Sakaida Isao
Creators Okita Kiwamu
Creator Keywords
Liver fibrosis Hepatic stellate cell N-acetyl- -cysteine LI90 COL1A2 promoter
Although recent studies suggest the inhibitory property of N-acetyl-L-cysteine (NAC) on activation of hepatic stellate cell (HSC), the effects on once-activated HSCs are not well clarified. We investigated the influences of NAC on human-derived once-activated HSC line, LI90 with a focus on the collagen α2 (I) (COL1A2) promoter expression. Plasmid containing whole length of COL1A2 promoter linked to firefly luciferase gene and its various 5′-deletions were transiently transfected to LI90. The luciferase activity was determined with or without 10 mM of NAC in the absence or presence of 1 ng/ml of transforming growth factor (TGF)-β. The effects of NAC on generation of intracellular reactive oxygen species (ROS) in LI90 were also analyzed. As a result, NAC significantly (P<0.05) suppressed the COL1A2 promoter expression in the absence or presence of TGF-β. The expression was much more inhibited when used the deletion containing only AP-1/NF-κB binding sites than that including only three SP-1 binding sites. The ROS production was also comparably inhibited by NAC in both condition. These results indicated NAC suppressed, through its anti-oxidative action, the COL1A2 promoter expression in once-activated HSCs in the absence or presence of TGF-β at least partly by affecting the signal transduction cascade encompassing AP-1/NF-κB activation.
Languages eng
Resource Type journal article
Publishers Elsevier
Date Issued 2002
File Version Not Applicable (or Unknown)
Access Rights metadata only access
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[ISSN]1386-6346
[NCID]AA11140867
info:doi/10.1016/S1386-6346(02)00089-X
[isVersionOf] [URI]http://www.sciencedirect.com/science/journal/13866346
Schools 医学部附属病院 大学院医学系研究科(医学)